In the past, glaucoma was regarded as a disease causing characteristic optic nerve disablement (optic nerve damage) due to ocular hypertension. However, an epidemiological research (“the Tajimi study”) conducted from 2000 to 2001 has revealed that the prevalence rate of normal-tension glaucoma (normotensive glaucoma) is significantly higher than that of hypertension glaucoma (high-tension glaucoma) in Japan compared with the Western countries. At present, glaucoma is defined as “a disease that involves distinctive changes in optic disc and the visual field and is marked by functional and structural abnormalities (disorders) in the eye in which optic nerve damage can ordinarily be alleviated and inhibited by sufficiently reducing intra-ocular pressure” (the Japan Glaucoma Society Guidelines for Glaucoma (3rd Edition)). Therefore, at present, the main purpose of glaucoma treatment is to reduce intra-ocular pressure. In addition, there have been attempts to develop neuroprotective agents in recent years. However, treatment of glaucoma involving the reduction of intra-ocular pressure has limitations. Thus, glaucoma is the leading disease in terms of the certification of physical disability caused by visual impairment in Japan.
Regarding glaucoma in the Western countries, the prevalence rate of high-tension glaucoma has been higher than that of normal-tension glaucoma and thus there has been little attention to normal-tension glaucoma. In the history of glaucoma, the possibility of the presence of normal-tension glaucoma was suggested. For example, “Duke-Elder's System of Ophthalmology” published in 1969 recites as follows: “It is to be remembered that an intra-ocular pressure that is generally accepted as being within the normal range may produce the typically pathological effects at the optic disc and in the visual fields when the nerve head is unduly vulnerable and may occur, for example, in myopic eyes; these cases properly come under the definition of glaucoma.” It is suggested that the reason for the high prevalence rate of normal-tension glaucoma in Japan is associated with myopia. However, there has been no specific explanation why optic disc is “fragile” in patients with myopia.
Optic Nerve Structure and Optic Disc Structure
Light enters into the eye and then is received by visual cells (the first neurons) so as to be converted into signals. The signals are further transmitted from bipolar cells (the second neurons) to ganglion cells. Axis cylinders of the ganglion cells serve as optic nerve fibers (the third neurons). The optic nerve fibers form a fascicle and the fascicle extends from optic disc outside the eye for signal transmission to the visual center of the brain.
Optic disc has a relatively oblong elliptical shape with a diameter of about 1.6 mm and is positioned on the nasal side of macula lutea (limbus luteus). About 1,200,000 axis cylinders of ganglion cells form a fascicle of optic nerve fibers such that the fascicle extends outside the eye. In addition, the central retinal artery and vein also extend through optic disc. When the fascicle of optic nerve fibers extends outside the eye, the optic nerve fibers run through 500-600 lamina pores of lamina cribrosa formed with connective tissue. When viewed from the exterior of the eye, the optic nerve is positioned on the nasal side of the eyeball in a horizontal view.
FIG. 2 shows a general image of a fascicle of optic nerve fibers extending through lamina cribrosa obtained by histological examination or scanning microscopic observation. However, there has been no literature about the anatomical role of lamina cribrosa as well as the morphological details thereof.